1. Field of the Invention
The present inventions deals with a botanical formulation made from the bark of a birch tree which can be used for the mitigation of conditions, diseases and disorders arising from, impacted by, or resulting in neurocutaneous malcircuitry.
2. Background
White Birch
White birch is a tree that is common to northern Europe and North America. It is known by its scientific name of Betula pendula or Betula alba. One of the chemicals isolated from birch bark is called betulin. Research suggests that betulin causes some types of tumor cells to start a process of self-destruction called apoptosis. Betulinic acid, which is made from betulin, has been studied as an anti-neoplastic agent. Betulinic acid has been reported to slow the growth of several types of tumor cells and may prove useful for treating several forms of cancer, including melanoma and certain brain cancers.
In 1994, scientists at the University of North Carolina reported that chemicals found in white birch bark slowed the growth of HIV. The following year, a researcher at the University of Illinois reported that betulinic acid killed melanoma cells in mice. Results from a German nonrandomized clinical trial published in 2006 indicated that birch bark extract may be an effective treatment for actinic keratosis, a pre-cancerous skin condition. Clinical trials are needed to determine what effect, if any, betulinic acid has in treating neoplastic disease in humans.
Some researchers think that birch bark has antimicrobial properties. For skin conditions, birch leaf tea has been used as a wash, and has been added to bath water. Birch bark and leaves have been applied directly to the skin without adverse effect. Birch oil is sometimes used in ointments or liniments and is considered a substitute for wintergreen. Birch bark is appreciated by cosmetic manufacturers for clearing the lumpy subcutaneous collections of fluid which appear as cellulite. Birch bark oil is marketed within the cosmetic industry for improving the cosmetic appearance of cellulite.
The bark, leaves, and buds from this and related birch trees are used in herbal and folk medicines on the skin to treat warts, eczema, and other skin conditions. The leaves are sometimes used on the scalp to help with hair loss and dandruff. Birch tar is used on the skin for skin irritations and parasites. Folk medicine advocates say that birch tea can be taken internally as a diuretic, mild sedative or as a treatment for rheumatism, gout, and kidney stones. Other claims for birch bark include the treatment of stomach problems, diarrhea, dysentery, and cholera. Native American Indians used birch bark for building canoes and for medicinal usage.
Some people drink fresh or bottled birch sap as a tonic. In Russia, birch bark has been consumed since 1834. In Europe, birch sap was fermented into beer, wine, and other spirits. The inner bark of birch was sometimes eaten as food. A sweetener, xylitol, is made from birch bark, and is safe for human consumption, even if diabetic. Birch bark tea can be made by steeping a teaspoon of the birch bark in a cup of boiling water for 15 minutes. Proponents recommend drinking from 2 to 5 cups of tea per day. Birch leaves are marketed for making teas. Birch bark flakes, powder, capsules, oil, sap, and liquid extracts are sold in herbal medicine shops and on the Internet. White birch bark is currently marketed as an FDA compliant nutritional supplement within the United States
Plants, including birch trees, can inflict rashes and allergic symptoms upon susceptible individuals. Persons sensitive to aspirin are advised to avoid birch products, because birch is known to possess aspirin-like compounds; however, toothpicks made of birch bark are not known to be dangerous to aspirin sensitive individuals. Aspirin-like compounds may pose a hazard to patients with poor kidney function, internal bleeding and to persons taking blood thinners; however, no actual example of such a hazard, relevant to white birch bark, has ever been reported in the medical literature. Until clinical safety data is available, consumption of white birch bark should not be recommended to individuals for whom aspirin is contraindicated or to pregnant women, nursing women and children.
Neurocutaneous Malcircuitry
Neurocutaneous malcircuitry is defined and discussed herein as extraneous neural conduction and/or transmission, as evidenced by intense, expanding or relentless pain, paresthesias, pruritus, swelling, bruising or inflammation, dysfunction and/or neural reflexes precipitated by cytokines and/or accumulated neurotransmitters.
Neurocutaneous malcircuitry is evidenced by extraneous neural conduction and/or transmission. Extraneous neural conduction is clinically identified when neural pathways route neural transmission in a fashion inconsistent with normal anatomic neurophysiology. A clinical example of this is of a patient who reflexively tears when her nose is touched after an inflammatory insult to the nose. Aberrant neural pathways (malcircuitry) may be capable of misdirection, interference, propagation and amplification of normal neural signals. Intuitively, normal impulses, if aberrantly conducted to the wrong target, may feedback upon themselves through reflex arcs, amplifying sensory impulses. A possible clinical example of this abnormal sensory amplification is the hyperesthesia of erythromelalgia. Misdirected neural impulses may stimulate autonomic and somatic reflex arcs, thus propagating aberrant transmission and resulting in new aberrant transmissions. Extraneous neural transmission clinically occurs when neural transmissions occur independently of normal neural reception, stimulation, moderation, and/or extinction. An example of an extraneous neural transmission is the pain impulse generated by aberrantly sustained reflexive muscular contraction, even after the original impulse inciting the pain is long gone.
Empirically, accumulated cytokines and neurotransmitters are instrumental in the development of neurocutaneous malcircuitry. Cytokines are released in response to pain, injury, illness, and inflammation. Cytokines cause changes in membrane permeability and vascular flow, resulting in fluid congestion and impaired lymphatic drainage. Neurotransmitters would be expected to accumulate within the synaptic clefts of congested tissue, escaping the clearance which is normally facilitated by diffusion. Failure of neurotransmitter clearance from the synapse is known to result in abnormal persistence of neural signaling.
Complex regional pain disorders, (also known as causalgia and reflex sympathetic dystrophy), are often associated with a history of a persistent or intensely painful inciting event. Analysis of clinical observation suggests that when pain signals exceed a certain neuro-electric threshold, action potentials spill outside the neuron's normal path of saltatory conduction, forming an extraneous neural pathway along other conductive areas (like the stream formed by a river from a heavy rain). If this aberrant neural pathway (stream) closes a connective loop with a ganglionic reflex arc, it could be capable of relentlessly feeding back upon itself. Intuitively, when neural transmissions are misdirected to a neural reflex arc, a new sensory transmission may result from the reflex itself, resulting in an extraneous neural transmission and potentially expanding the neural malcircuitry.
It is well accepted that normal neural transmission may be misdirected by neural malcircuitry to the wrong target. Abnormal transmission may target any structure, function, or system of the body, depending upon the path of neural conduction. Inappropriate sweating, movement, vascular flow, or a host of other disruptions may ensue from neural transmission misdirected through extraneous neural circuits. For example, a female patient presented with a history of a laceration to the nasal sidewall from a motor vehicle accident years earlier. Ever since the laceration healed, light touch to her, still numb, nose resulted in intense pain of her cheek, with reflexive tearing from her right eye. One possible explanation is that cutaneous nerves were severed and inappropriately reconnected. However, the laceration did not physically include areas known to be innervated for the resulting sensation and reflexes (the right cheek, tear glands and tear duct are not “hard wired” from the nose).
It is unknown how neural cell bodies themselves may be incorporated in the abnormal conduction pathways of aberrant neural circuitry. But clinical examples of neurocutaneous malcircuitry demonstrate complete and instantaneous restoration of normal neural function when aberrant neural transmission is terminated. This suggests that normal nerve cell bodies are not harmed by participation within cytokine induced neural malcircuitry.
Neural Function Circuitry & Reflexes
Traditionally, neurotransmitters must be removed from the synapse for signal extinction. Signal extinction is accomplished at the neuromuscular junction by a) acetylcholinesterase which degrades and inactivates acetylcholine, b) cell uptake of the neurotransmitter; and c) simple diffusion.
The over-accumulation of the neurotransmitter, acetylcholine, within the synaptic cleft at the neuromuscular junction, results in failure of neural impulses to extinguish normally. A potentially lethal example of this is pesticide poisoning. Pesticides inactivate acetylcholinesterase, causing failure of enzymatic degradation of acetylcholine. Resultant over-accumulation of acetylcholine at the neuromuscular junction causes neural impulses to fail to extinguish normally. This results in sustained muscle contraction which freezes the muscles needed for vital functions.
It appears that neurotransmitters are not normally cleared from the neuromuscular junctions of patients suffering from conditions of neurocutaneous malcircuitry, but if acetylcholinesterase deficiency was the culprit, anti-cholinergic medications would be very helpful, yet they are not. Lack of neurotransmitter clearance by diffusion and/or cell uptake is likely culpable for extraneous neural transmissions, but there is more to this story. Aberrant neural reflexes of complex regional pain disorders, such as erythromelalgia, are known to progressively expand outside the region relevant to the inciting injury. Unbridled neural reflexes are to blame for much of the chaos of erythromelalgia. The brain is responsible for moderating normal reflexes, but fails to appropriately respond to the malcircuitry precipitated by inflammatory cytokine accumulation.
The peripheral nervous system receives sensory afferent signals from cutaneous nerves, and transmits these neural impulses to the spinal cord, where the signal is further transmitted to the brain. Reflexes work a little differently. Reflex impulses are routed through the dorsal root ganglion and into the spinal cord, where the nerve synapses with an efferent nerve and a motor transmission is automatically generated (ex: the knee jerk reflex when stretch receptors of the knee are stimulated). The brain, via the spinal cord, receives feedback relative to the stimulation of the stretch receptors, as well as to the dorsal horn's resultant muscular activity (the knee “jerk”). The brain processes the precise measure of inhibitory response required to moderate and extinguish the knee jerk reflex. The brain moderates reflexive response by inhibitory neural feedback transmitted through the descending inhibitory spinothalamic track (DIST). If the brain is damaged, hyper-reflexia may result due to inadequate inhibition of normal reflex arcs. For example, hyper-reflexia often results from the brain damage of hypertonic cerebral palsy. In contradistinction, normal inhibitory regulation of a healthy brain may fail to extinguish reflexes which have been altered by neurocutaneous malcircuitry.
The descending inhibitory spinothalamic track (DIST) is housed within the central nervous system, coursing from the brain through the spinal cord. Normally, neural reflex circuits between the peripheral nervous system and the DIST are subject to moderation and extinction by the brain. Clinically, the hyper-reflexia of neurocutaneous malcircuitry suggests that reflexes conducted along extraneous neural pathways are not well moderated by the DIST. In fact, neural transmission along cytokine induced neurocutaneous malcircuitry may actually incorporate the DIST, looping back and involving the brain in this messy malcircuitry. It is conceivable that cytokine induced neurocutaneous malcircuitry is involved in the manifestation of migraines, attention deficit disorder, autism, neuropsychiatric disease, and a host of other possible diseases.